Colorectal cancer (CRC) is one of the most common malignancies in the world. Studies have demonstrated that single nucleotide polymorphisms (SNPs) in microRNA genes (miRSNPs) are involved in the occurrence of cancers. However, the relationship between the miRSNPs within the terminal-loops of microRNA precursors and the development of CRC is still largely unknown. In this study, we found that a miRSNP rs7911488 T>C in the terminal-loop of pre-miR-1307 was significantly associated with the occurrence of CRC. The C allele of rs7911488 is more prevalent in CRC patients than in healthy controls (P < 0.001), and this C allele prevalence is related to low level of miR-1307 expression. A RNA-binding protein MBNL1 binds with a 'UGCUGC' motif in the terminal-loop of the C-allelic pre-miR-1307 and blocks Dicer processing, resulting in downregulation of miR-1307 expression. Consequently, the antiapoptosis protein Bcl2, which is a direct target of miR-1307, is overexpressed in CRC. Furthermore, MBNL1 participates in processing of both C-allelic and T-allelic pre-miR-1307. In summary, our results show that rs7911488 C-allelic pre-miR-1307 binds to MBNL1 and infers with Dicer processing, leading to reduced miR-1307 and increased Bcl2 expression, thus representing an important process in the initiation of CRC.

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Competitive adsorption of As(V) and Sb(V) at environmentally relevant concentrations onto ferrihydrite was investigated. Batch experiments and XPS analyses confirmed that in a binary system, the presence of Sb(V) exhibited a slight synergistic effect on As(V) adsorption. XPS analyses showed that As(V) and Sb(V) adsorption led to obvious diminishment of Fe-O-Fe and Fe-O-H bonds respectively. At pH of 9, a more significant decrease of Fe-O-Fe was observed in the binary system than that in a single system, indicating that As(V) displayed an even stronger interaction with lattice oxygen atoms under competitive conditions. Basically, ionic strength demonstrated a negligible or positive influence on As(V) and Sb(V) adsorption in binary system. Study of adsorption sequence also indicated that the presence of Sb(V) showed a promotion effect on As(V) adsorption at neutral pHs. Considering that co-contamination of As and Sb in waters has been of great concern throughout the world, our findings contributed to a better understanding of their distribution, mobility, and fate in environment.

Objectives. Breast cancer is the most common malignant tumor among females, and miRNAs have been reported to play an important regulatory role in breast cancer progression. This study aimed to explore the function and underlying molecular mechanism of miR-301b-3p in breast cancer. Methods. Differential analysis and survival analysis were performed based on the data accessed from the TCGA-BRCA dataset for identification of the target miRNA. Bioinformatics analysis was conducted to predict the downstream target gene of the miRNA. Real-time quantitative PCR was carried out to detect the expression of miR-301b-3p and nuclear receptor subfamily 3 group C member 2 (NR3C2). Western blot was used to assess the protein expression of NR3C2. Cell counting kit-8 assay was performed to evaluate the proliferation of breast cancer cells. Transwell assay was conducted to determine the migratory and invasive abilities of breast cancer cells. Dual-luciferase reporter assay was employed to verify the targeting relationship between miR-301b-3p and NR3C2. Results. miR-301b-3p was elevated in breast cancer cell lines and promoted cell proliferation, migration, and invasion in terms of its biological function in breast cancer. NR3C2 was validated as a direct target of miR-301b-3p via bioinformatics analysis and dual-luciferase reporter assay, and NR3C2 was downregulated in breast cancer cell lines. The rescue experiment indicated that NR3C2 was involved in the mechanism by which miR-301b-3p regulated the malignant phenotype of breast cancer cells. Conclusion. The present study revealed for the first time that miR-301b-3p could foster breast cancer cell proliferation, migration, and invasion by targeting NR3C2, unveiling that miR-301b-3p is a novel carcinogen in breast cancer.